PMID- 30533546
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220330
IS  - 2405-8440 (Print)
IS  - 2405-8440 (Electronic)
IS  - 2405-8440 (Linking)
VI  - 4
IP  - 11
DP  - 2018 Nov
TI  - IL-33 suppresses GSK-3beta activation through an ST2-independent 
      MyD88/TRAF6/RIP/PI3K/Akt pathway.
PG  - e00971
LID - 10.1016/j.heliyon.2018.e00971 [doi]
LID - e00971
AB  - AIMS: The present study was conducted to explore the effect of interleukin-33 
      (IL-33) on glycogen synthase kinase-3beta (GSK-3beta) activation involving Tau 
      phosphorylation, a critical causative factor for Alzheimer's disease (AD). MAIN 
      METHODS: Experiments were performed using PC-12 cells. Target proteins were 
      knocked-down by transfecting with the siRNA for each protein. The kinase 
      activities were assessed by monitoring phosphorylation of Thr308 and Ser473 for 
      Akt and phosphorylation of Ser9 and Tyr216 for GSK-3beta in the Western blotting. 
      KEY FINDINGS: Exogenously applied IL-33 activated Akt and inactivated GSK-3beta. 
      IL-33-induced Akt activation and GSK-3beta inactivation were significantly inhibited 
      by knocking-down myeloid differentiation factor 88 (MyD88), tumor necrosis factor 
      receptor associated factor 6 (TRAF6), receptor-interacting protein (RIP), or 
      phosphatidylinositol 3 kinase (PI3K). IL-33 neutralized amyloid beta(1-42) 
      (Abeta(1-42))-induced Akt inactivation and GSK-3beta activation. SIGNIFICANCE: The 
      results of the present study show that IL-33 inactivates GSK-3beta through an 
      ST2-independent MyD88/TRAF6/RIP/PI3K/Akt pathway and inhibits Abeta(1-42)-induced 
      GSK-3beta activation. This suggests that IL-33 could restrain GSK-3beta-mediated Tau 
      phosphorylation in AD.
FAU - Nishizaki, Tomoyuki
AU  - Nishizaki T
AD  - Shanghai University of Traditional Chinese Medicine, Education College of 
      Medicine, Osaka, 530-0047, Japan.
AD  - Innovative Bioinformation Research Organization, Kobe, 651-1223, Japan.
LA  - eng
PT  - Journal Article
DEP - 20181126
PL  - England
TA  - Heliyon
JT  - Heliyon
JID - 101672560
PMC - PMC6260469
OTO - NOTNLM
OT  - Biochemistry
EDAT- 2018/12/12 06:00
MHDA- 2018/12/12 06:01
PMCR- 2018/11/26
CRDT- 2018/12/12 06:00
PHST- 2018/10/05 00:00 [received]
PHST- 2018/11/14 00:00 [revised]
PHST- 2018/11/21 00:00 [accepted]
PHST- 2018/12/12 06:00 [entrez]
PHST- 2018/12/12 06:00 [pubmed]
PHST- 2018/12/12 06:01 [medline]
PHST- 2018/11/26 00:00 [pmc-release]
AID - S2405-8440(18)36381-3 [pii]
AID - e00971 [pii]
AID - 10.1016/j.heliyon.2018.e00971 [doi]
PST - epublish
SO  - Heliyon. 2018 Nov 26;4(11):e00971. doi: 10.1016/j.heliyon.2018.e00971. 
      eCollection 2018 Nov.